Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Posterior Seg > Retinal Blood Vessel Anomalies > Flashcards

Retinal Blood Vessel Anomalies Flashcards

1
Q

Minimal systemic workup

A
  1. Blood pressure, respirations, and pulse (vitals)
  2. CBC with diff
  3. Ausculation of carotid arteries. Listening.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Low RBC count could indicate

A 
Anemia 
BM failure 
Kidney disease
hemolysis 
Bleeding 
Leukemia 
Malnutrition 
Vitamin Def 
Pregnancy 
Medication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

High RBC count could indicate

A

Congenital heart disease
Dehydration
Renal cell carcinoma
Polycythemia vera- slow growing blood cancer. BM makes too many–> thickens blood –> Clots –> MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Low WBC count could indicate

A

Severe infections
Meds that destroy WBC
Autoimmune disorders that distort WBC- lupus, RA
Viral infections
Congenial disorders that involve diminished BM function
Reaction to meds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

High WBC count could indicate

A

An increased production of WBC to fight an infection (bacterial or viral)
Disease of BM causing high production of WBC (leukemia)
Reaction to drug
Autoimmune disease that increases WBC production (RA)
Severe allergic reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Micro-aneurysms

  • How big?
  • What is it?
A

50-100 microns in size

Microscopic ballooning of the capillary vasculature. Occurs in a reqs of hypoxia secondary to capillary destruction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Micro-aneurysms are easily observable with ___

A

IVFA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Micro-aneurysms result from

A

Acute hypoxia of the deep capillary network.

Layer involved- INL.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Patters of Micro-aneurysms

A

focal, local (1), or clustered like grapes on a vine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Can micro aneurysms spontaneously resolve?

A

Yes, may leak at first but later may spontaneously seal secondary to hyalinization.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What 3 things are signs of active micro aneurysms leakage?

A

Dot blot hemorrhages, exudate, and edema.

See this? Micro aneurysm have been there a while

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Expected visual outcomes of Micro-aneurysms

A

Good unless near FAZ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Micro-aneurysms treatment options

A

Laser photocoagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What do Micro-aneurysms look like using IVFA

A

Starry night.

Hyper fluorescing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Macro-aneurysm

-What is it and what area of the retina is it associated with?

A

Isolated ballooning of a larger or major retinal blood vessel. Usually artery or arteriole.

Focal/local blood vessel damage.

Multiple layers of retina may be involved- multi level hemorrhage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

3 outcomes of Macro-aneurysms

A

Chronic leakage

Rupture of aneurysm- acute hemorrhage. Can involve multiple layers of retina and vitreous.

Spontaneous resolution- Similar to microaneurysms. They can seal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Visual outcomes of macro aneurysms

A

Depends on location and amount of edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Treatment options for macro aneurysms

A

Depends on location/if macula is involved.

Ex: If in periphery and no VA changes, monitor every 3 months and refer to PCP

Laser or anti veg F

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Micro aneurysms usually involve the __ capillary network

Macro usually involve ____

A

Deep

Arteries or arterioles found in the NFL (can dip down a bit)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

3 groups of Idiopathic Juxtafoveal Telangiectasia

A
  1. Aneurysmal
  2. Parafoveal
  3. Occlusive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Idiopathic Juxtafoveal Telangiectasia: Aneurysmal (group 1)

  • Demographics
  • due to what
  • Changes to retina/vision
A

Healthy, young males
Abnormal glucose tolerance
Mild to moderate unilateral VA loss with macular cystic changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Idiopathic Juxtafoveal Telangiectasia: Aneurysmal. (group 1)

Ocular findings?

A
  • Unilateral macular edema with cystic changes.
  • Temporal fovea is involved.
  • Telangiectasia- spider like. Dip down at right angle into deeper retina.
  • Micro Aneurysms and venule changes
  • Lipid deposition (exudate) with chronic leakage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How to treat Idiopathic Juxtafoveal Telangiectasia: Aneurysmal. (group 1)

A

Photocoagulation

Anti VEGF therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Idiopathic Juxtafoveal Telangiectasia: Parafoveal group 2

Presentation?

  • Demographics
  • Due to what
  • unilateral or bilateral
  • Compare to IJT group 1
A

Healthy middle age males and females
Due to abnormal glucose tolerance
Bilateral vision loss with macular atrophy
More common and worse prognosis as compared to IJT-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

IJT group 2 Parafoveal Ocular findings

A

Grayish loss of juxafoveal retinal transparency
Temporal early, but then surrounds entire fovea
Fine crystalline depositions and RPE hyperplasia
Micro- A and neovsac with macular edema.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

IJT group 2 parafoveal treatment options

A

Anti VEGF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q 
IJT group 3 occlusive 
Presentation 
-How common? 
-Associated with 
-Loss of what vision 
-How does it affect the ON?
A

Very rare condition with poor VA outcomes
Associated with systemic disease or neurological disease. (polycythemia vera, multiple myeloma, CLL)
Loss of central vision
Ocular atrophy impacts peripheral vision as well.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Difference between IJT group 1 and 2

  • Demographics
  • unilateral or bilateral?
  • Amount of VA loss
  • Neovasc present?
  • How common?

Similarities

A 
Group 1: 
Males
Unilateral
Vision loss less severe
No novas
Less common
Group 2:
Males and females 
Bilateral 
VA loss more severe 
Neovasc prob due to ischemia 
More common

Similarities:
Edema and exudate
Involve macula
Due to glucose intolerance (G3 is more systemic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Collateral blood vessels - What are they and where do they develop?
Difference between collateral and neovasc?

A

They develop within the framework of the existing vessel network.
May develop vein to vein, artery to artery, or artery to vein.

They are beneficial, unlike neovasc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Collateral blood vessels location in the retina

A

Located on or within the superficial retina.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Collateral blood vessels represent

A

Past or present regional vascular compromise.
Could be
artery to artery connection (due to artery damage)
Vein to vein connection (due to vein damage)
Artery to vein connection (due to capillary damage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Optocillary shunt

A

Collateral blood vessels located on the surface of the ON.

Due to:

  1. Could be associated with orbital mass. Do MRI to see if it’s due to pressure.
  2. Could be due to past or present regional vascular compromise.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is congenital shunt vessels or artery-vein communication?

A

AV communication without capillary obstruction or compromise is a shunt vessel.
Congenital- has alwaysys been there.

No additional testing.
Prob Dx of exclusion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Should collateral vessels leak?

A

NO! They should not. They are a closed system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is highly associated with collateral vessels?

A

Retinal vein occlusion

or congenital- AV communication/shunt

36
Q

What does IRMA stand for

A

Intra retinal vascular abnormalities

37
Q

How is IRMA similar to collateral blood vessels?

A

No leakage

38
Q

What is IRMA

A

AV connections that BYPASS capillary networks.
Will see fine, irregular, red BV that run from arterioles to venues. They will run over capillary non perfusion due to drop out.
Tells us that there is been capillary drop out.

39
Q

IRMA location

A

In areas of non-perfusion in diabetic retinopathy only.

40
Q

IRMA is precursor to

A

Severe diabetic eye disease.

41
Q

How to differentiate between collateral blood vessels and IRMA?

A

Think IRMA if pt is diabetic
IRMA is arteriole to venule only

Collateral can be artery-artery, vein-vein, or artery-vein.

42
Q

Neovascularization

A

New blood vessel growth as a response to hypoxia.
Secondary to capillary non-perfusion.
Vessels are weak, leaky, and associated with fibrosis.
Fibrosis develops due to hypoxia and inflammation. Could cause tractional changes.

43
Q

Neovascularization is associated with

A

Fibrosis and VEGF.

44
Q

Three types of Neovasc

A

NVI- Neovasc of the iris. At pupillary frill or angle.

NVD- neovasc of the disk. May lead to vitreous hemorrhage. Faces ischemic area. On nerve or 1DD away.

NVE- Neovasc elsewhere. Between junction of perfused to non perfused tissue. Faces hypoxic retina. Multiple layers involved.

45
Q

Neovasc expected retinal findings.

A

Retinal edema- may be hard to tell where it starts and ends since many layers may be involved.

Hemorrhage- retinal (due to NVE) or vitreous (due to NVD)

Fibrosis and traction- Fibrosis occurs due to hypoxia, inflammation and GF. Neovasc can grow in and around the scar tissue. Overtime, scar tissue shrinks and can pull on the retina. May cause tractional retinal detachment

46
Q

Ischemia leads to the development of

A

neovasc

47
Q

Gold standard to look at neovasc

A

IVFA

48
Q

Neovasc

  • Visual outcomes?
  • Strong association with
  • Tx options
A

Unsure. Depends on acute vs chronic (fibrosis –> traction)
Strong association with uncontrolled systemic disease such as DM. Could also be due to BRVO, CRVO, or hemi retinal occlusion.

Pan retinal laster photocoagulation (PRP)
anti VEGF therapy

49
Q

Which vessels are more likely to become tortuous?

A

Veins- loosely attached to the retina.

Arteries are more ridged due to muscle and are tightly attached to the retina. Less likely for these to become tortuous.

50
Q

Technology and imaging for collateral blood vessels

A

IVFA- identify collateral vessels. Should not leak. Could help identify a BRVO.
OCTA- helps identify neovascularlization
Possible MRI if optocilliary shunt- rule out orbital mass.

51
Q

Expected outcomes and resolution of collateral blood vessels

A

If blood flow is re-established, collateral vessels will regress.

52
Q

Doing IVFA. How long should it take to see initial filling? what if it takes longer>

A

15-25 seconds. Should be uniform.
If slow, indicates blockage- carotid blockage or hyperlipidemia.
If one quadrant doesn’t fill as fast, could be due to BRVO.

53
Q

Difference & similarity between collateral vessels and IRMA

A

IRMA is arteriole to venule ONLY and exclusive to diabetic eye disease!

Collateral vessels can be artery-artery, vein-vein, or artery-vein.

*Both have no leakage.

54
Q

Diagnostic testing for IRMA

A

IVFA to identify leaking. If leaking, no IRMA. Prob neovasc.

OCT to identify structural changes in the retina.

OCTA identifies neovasc, IRMA, or collateral.

55
Q

NVI

  • Who is susceptible to develop?
  • Location
A

Pts with branch vein occlusion, or pt with significant diabetic eye disease.

Location- Pupillary frill or in angle.
Will see neo

56
Q

NVD

  • Location
  • Where it is relative to healthy retinal
  • Could lead to _____. Why?
A

On the disc or within 1DD from the ONH.
Neo develops at the boarder of healthy: hypoxic tissue. Faces hypoxic zone.
Could lead to virtual hemorrhage because the ILM is very thin/non existent at the ON. Neovasc could grow into the vitreous, along with fibrosis and bleed.

57
Q

NVE

  • Location
  • What layers of retina involved?
A

Anywhere other than iris or on the ONH/within 1 DD

Multiple layers of retina involved

58
Q

Fibrosis occurs due to which 3 things

A

Hypoxia, inflammation, and GF.

59
Q

Retinal hemorrhage is likely to happen with what kind of neo?

A

NVE

60
Q

Virtual hemorrhage is likely to happen with what kind of neo?

A

NVD- ILM is thin/absent there. Neo can easily enter the vitreous and bleed.

61
Q

Why does neovascularization occur?

A

When the balance between angiogenesis inhibitors and stimulators is altered. Usually disrupted due to hypoxia.
Ex: BRVO? Off the chart amount of VEG-F released into the retina.

AKA ischemia leads to development of neovasc. (also prob flame shape hems, and CWS)

Look for neo with IVFA.

62
Q

Acquired vein tortuosity is associated with (3)

A
  1. Venous stasis (back flow of blood)
  2. Retinal hypoxia
  3. Localized vascular occlusion.
63
Q

Acquired vein tortuosity could be due to

A

BRVO, CRVO, hemi retinal vein occlusion

Diabetic retinopathy

64
Q

Most common cause of blood vessel tortuosity

A

Usually congenital

65
Q

How do you know if blood vessel tortuosity is congenital?

If so, expected visual outcomes and treatment options?

A

Involves extreme changes in all 4 quadrants OU. Involving both veins and arteries.

Good visual outcomes- no changes.
Monitor.

66
Q

Equation to calculate total cholesterol (TC)

A

TC= HDL + LDL + VLDL

calculate VLDL by triglyceride level divided by 5

67
Q 
Magic numbers for 
TC (total cholesterol) 
LDL
HDL
Triglycerides
A

TC (total cholesterol) = less than 200 (can be higher if pt has high HDL levels)
LDL= Less than 100
HDL= 40-60
Triglycerides = less than 150

68
Q

Lipid profile ratio you need to calculate to get good idea of cholesterol level

A

TC/HDL

If HDL levels are high (which is good), it can make total cholesterol levels look high.

Do this ratio to make sure levels are normal.

Males should be less than 5
Females less than 4.4

69
Q

Vascular sheathing
Congenital vs acquired
-list locations and which vessels it is associated with

A

Congenital- Artery and vein sheathing is common. Usually located 2DD of the ON or at ON. arteries AND veins involved.

Acquired vein sheathing- Retinal periphery. Looks like a halo. Associated with periphlebitis. (inflammation of outer coat of a vein)

Acquired artery sheathing- Associated with arteriosclerosis. Silver/copper wire appearance.

70
Q

Congenital vascular sheathing

  • What vessels are involved
  • Location
A

Artery and vein sheathing is common. Usually located 2DD of the ON or at ON. arteries AND veins involved.

Check to see if there is any sign of papilledema, papillitis, and papillophlebitis. Will see these signs if acquired, but usually congenital.

71
Q

Acquired vein sheathing

  • location
  • Looks like what?
  • Associated with
A

Retinal periphery. Looks like a halo. Associated with periphlebitis. (inflammation of outer coat of a vein) `

Periphlebitis due to systemic cause such as: posterior uveitis, MS, lupus, Sarcoidosis, pars planets, toxoplasmosis, RP, RVO.

72
Q

Acquired artery sheathing

  • Looks like what?
  • Associated with
A

Associated with arteriosclerosis. Silver/copper wire appearance.

73
Q

Lipemia Retinalis

  • Due to what
  • Appearance and location
A

Elevated serum triglyceride levels. Can range from 2500-20,000. (Normal is less than 150) Causes retinal blood vessels to fill with lipids= creamy salmon color.

Begins in the periphery then slowly involves vessels in PP.

74
Q

Visual outcomes of lipemia retinals

A

Asymptomatic, no VA loss. Prob have systemic disease- could have stroke, MI.

Also want to have family members checked- genetic

75
Q

Persistent hyaloid membrane- Bergmeister’s papilla

  • What is it?
  • Location ?
  • Symptoms ?
  • Prognosis/management
A

Incomplete regression of the hyaloid artery and embryonic glial sheath. Congenital.

Usually located at the nasal margin.

Asymptomatic.

Good prognosis, no change in VA. Monitor.

76
Q

See persistent hyaloid membrane. Need to rule out what?

A

PHPV- persistent hyper plastic primary vitreous
Retinoblastoma
ROP- ask about prematurity

77
Q

Pre-papillary vascular loops. What are they? Symptoms ?
Artery or vein?
Bilateral or unilateral?

A

Congenital.

retinal blood vessel that projects into the vitreous (1.5mm) from the ON and returns to the ON.

usually arterial and unilateral.

True extension of the central retinal artery- independent of bergmeister papillae, but may have glial tissue wrapped around it.

Asymptomatic.

Have pt change gazes, it will move around in the eye.

78
Q

Pre-papillary vascular loop needs to monitored in case it leads to?
What are other differential diagnosis?

A

Vitreous hemorrhage or RAO

Acquired loops, tumors, or collateral blood vessels.

79
Q

Congenital macrovessels

  • What is it?
  • Location
  • symptoms
A

Abnormally large retinal vessel that crosses over the horizontal raphe

Usually a vein or venule

Easily observed!

Asymptomatic

80
Q

Congenital macrovessels. Treatment and prognosis

A

Look for retinal edema if leakage.
OCTA, OCT, IVFA

No treatment unless there is leakage.
Good prognosis, rule out differentials such as Racemose Angioma.

81
Q

Racemose angioma

  • What is it?
  • Symptoms
A

Macro vessel that enters and exists the optic nerve.
AV malformation

Large and tortuous vessel.

Symptoms depend on location or hemorrhage. Usually have VA loss and are aware of CNS disorder. Will likely have systemic signs such as seizures/hemiporesis

82
Q

Treatment and prognosis of racemose angioma

A

Refer to neuro. They also need MRI.

Usually have symptoms- VA loss or systemic such as seizures.

83
Q

Cilio retinal vessel

  • Congenital?
  • How common
  • ARtery or vein
A

Congenital, seen in 25% of patients.

Artery

84
Q

Cilio retinal vessel is derived from what artery

A

Short posterior ciliary arteries. Rarely choroidal vasculature. AKA blood not coming from central retinal artery- good if there is CRAO.

85
Q

Cilio retinal vessel appearance and symptoms

A

Hooks out of rim tissue from temporal edge and moves towards the macula.
Completely asymptomatic

Posterior Seg (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions